Percutaneous ventricular assist devices are increasingly being utilized in patients with acute myocardial infarction and cardiogenic shock. Herein, we discuss the mechanism of action and hemodynamic effects of such devices. We also review algorithms and best practices for the implantation, management and weaning of these complex devices.
Cardiogenic shock is defined as persistent hypotension, accompanied by evidence of end organ hypo-perfusion. Percutaneous ventricular assist devices (PVADs) are used for the treatment of cardiogenic shock in an effort to improve hemodynamics. Impella is currently the most common PVAD and actively pumps blood from the left ventricle into the aorta. PVADs unload the left ventricle, increase cardiac output and improve coronary perfusion. PVADs are typically placed in the cardiac catheterization laboratory under fluoroscopic guidance via the femoral artery when feasible. In cases of severe peripheral arterial disease, PVADs can be implanted through an alternative access. In this article, we summarize the mechanism of action of PVAD and the data supporting their use in the treatment of cardiogenic shock.
Cardiogenic shock (CS) is defined as persistent hypotension (systolic blood pressure <90 mmHg for >30 minutes, or the need for vasopressors or inotropes), end-organ hypo-perfusion (urine output <30 mL/h, cool extremities or lactate > 2 mmol/L), pulmonary congestion (pulmonary capillary wedge pressure (PCWP) ≥ 15 mmHg) and decrease cardiac performance (cardiac index <2.2 )1,2 due to a primary cardiac disorder. Acute myocardial infarction (AMI) is the most common cause of CS3. CS occurs in 5-10% of AMI and historically has been associated with significant mortality3,4. Mechanical circulatory support (MCS) devices such as intra-aortic balloon pump (IABP), percutaneous ventricular assist devices (PVAD), extracorporeal membrane oxygenation (ECMO) and percutaneous left atrial to aortic devices are frequently used in patients with CS5. Routine use of IABP has demonstrated no improvement in clinical outcomes or survival in AMI-CS1. Given the poor outcomes associated with AMI-CS, the difficulties in conducting trials in AMI-CS, and the negative results of IABP use in AMI-CS, clinicians are increasingly looking to other forms of MCS.
PVADs are increasingly utilized in patients with AMI-CS6. In this article, we will focus our discussion primarily on the Impella CP, which is the most common PVAD used currently6. This device utilizes an axial flow Archimedes-screw pump which actively and continuously propels blood from the left ventricle (LV) into the ascending aorta (Figure 1). The device is most frequently placed in the cardiac catheterization laboratory under fluoroscopic guidance via the femoral artery. Alternatively, it can be implanted through an axillary or transcaval access when necessary7,8.
This protocol is the standard of care in our institution.
1. Insertion of the PVAD (e.g., Impella CP)
2. Post-procedural care
3. Positioning
4. Weaning
5. Removal12
Table 1 shows the safety and efficacy of PVAD implantation35,36,37,38,39,40.
Optimizing PVAD Outcomes
PVADs are a resource-heavy intervention that requires significant experience and expertise to optimize outcomes. The following best practices should be considered:
1. Utilizing PVAD early after shock onset
2. Utilizing PVAD prior to escalating doses of vasopressors and inotropes
3. Utilizing PVAD prior to PCI
4. Utilizing invasive hemodynamics for PVAD escalation and de-escalation
5. Minimizing PVAD complications
6. Utilizing Shock Protocols
Utilizing PVAD early after shock onset
AMI-CS is caused by coronary ischemia leading to diastolic failure, increasing LV wall tension, systolic failure and systemic hypo-perfusion. If not promptly treated, CS results in lactic acidosis, end-organ failure and death3. It is imperative to support patients prior to the onset of refractory shock. Patients in refractory shock go on to develop systemic inflammatory response syndrome, triggering a cascade of neurohormonal changes which are difficult to reverse3. This was demonstrated in the cVAD registry where patients who received MCS early, with a duration of shock before PVAD initiation of <1.25 hours, had higher survival to discharge compared with those who received PVAD after 1.25 hours16. This was also demonstrated by Tehrani et al. who demonstrated that for patients requiring PVAD, every 1-hour delay in escalation of therapy was associated with a 9.9% increased risk of death17.Notably, small randomized controlled trials which compared IABP to PVADs demonstrated a superior hemodynamic effect, but not a mortality benefit18,19.
Utilize PVAD prior to escalating doses of vasopressors and inotropes
Use of vasopressors and inotropes is typically needed in patients presenting with AMI-CS. These medications rapidly improve blood pressure and cardiac output. Unfortunately, they also increase heart rate and afterload, resulting in increasing myocardial oxygen consumption and work20. They are also associated with increasing arrythmogenicity and infarct size. Given these hemodynamic effects, PVADs should be considered at the time of initiation of an inotrope or vasopressor and/or when escalating their use in patients with AMI-CS. This was demonstrated in the cVAD registry where the rate of survival to discharge was inversely proportional to the amount of inotropic support used before initiation of MCS. Patients who received 0, 1, 2, 3, or 4 or more inotropes had a 68%, 45%, 35%, 35%, and 26% rate of survival to discharge, respectively (odds ratio 2.3, 95% confidence interval 0.99 to 5.32, p=0.05)21.
Utilize PVAD pre-PCI in AMI-CS
PCI causes a transient cessation of blood flow resulting in increasing LV volume and decreasing systolic pressure. In patients with normal LV function, these physiologic changes are typically transient and quickly recover. In patients with poor LV reserve and those presenting in AMI-CS, the physiologic effects of PCI can be catastrophic. PCI can also result in micro-embolization and reperfusion injury resulting in infarct zone expansion. Early initiation of hemodynamic support prior to PCI has been shown to improve outcomes in patients with AMI-CS. The USPella registry (n=154) demonstrated survival to discharge was significantly higher in the group which received PVAD pre-PCI as compared to post-PCI (65% vs 40%, p=0.01, OR =0.37 CI 0.19-0.72)22. In the cVAD registry, an analysis of 287 patients demonstrated that MCS implantation before PCI was independently associated with improved survival16. Lastly in the IQ database, analysis of 5,571 patients demonstrated that PVAD use pre-PCI was associated with improved survival21.
Utilizing invasive hemodynamics to PVAD management
Use of invasive hemodynamic monitoring with pulmonary artery catheters has been associated with improved outcomes in AMI-CS patients requiring PVAD. PA catheters help to guide the effectiveness of PVAD, the need for MCS escalation, the identification of RV failure as well in aiding weaning of such devices21. In a retrospective cohort study of the national inpatient sample, patients with PA catheters who were admitted with AMI-CS had decreased mortality and lower in-hospital cardiac arrest23. Tehrani et al also demonstrated that use of a PA catheter, along with a standardized cardiogenic shock protocol, was associated with a 39% absolute increase in survival (71% vs. 32.0%; p < 0.01)17. Recent data published from the cardiogenic shock working group also demonstrated a benefit in mortality when PA catheters were used24. PA catheters allowed for serial monitoring of cardiac function by parameters such as cardiac power output (), right atrial pressure and PAPI (), which are important predictors of outcomes in AMI-CS16,25. PAPI, like many measures of RV function, is sensitive to loading conditions, and varies by population of patient (e.g., chronic heart failure vs pulmonary hypertension vs ACS)26. In the future, a more specific PAPI cut off may be provided in AMI-CS versus other conditions such as chronic advanced heart failure or post LVAD or cardiac transplant implantation26. It is our clinical practice to use <1.0 as the cut off for consideration of right ventricular support in AMI-CS patients27.
Figure 1: PVAD, Detailed Anatomy and Hemodynamic Effects. (A) Detailed anatomy of a PVAD (This figure has been modified from Abiomed). (B) Hemodynamic effects of PVAD. CPO: cardiac power output, O2: oxygen, MAP: mean arterial pressure, PCWP: pulmonary capillary wedge pressure, LVEDP: left ventricular end diastolic pressure, LVEDP: left ventricular end diastolic pressure. Please click here to view a larger version of this figure.
Figure 2: A Shock Protocol. The algorithm for the National Cardiogenic Shock Initiative. AMI: acute MI, NSTEMI: non-ST elevation myocardial infarction, STEMI: ST-elevation myocardial infarction, LVEDP: left ventricular end diastolic pressure, MAP: mean arterial pressure, CO: cardiac output, sPAP: systolic pulmonary artery pressure, dPAP: diastolic pulmonary artery pressure, RA: right atrial pressure Please click here to view a larger version of this figure.
Study | Patient Population | N | Devices Compared | Findings |
Seyfarth et al | Acute myocardial infarction and Cardiogenic Shock | 25 | IABP vs Impella 2.5 | No device-related technical failure |
Non-statistically significant ↑pRBC transfusion in Impella group | ||||
Non-statistically significant ↑FFP in Impella Group | ||||
↑Hemolysis in Impella group | ||||
No difference in mortality or LVEF | ||||
Schrage et al. | Acute myocardial infarction and Cardiogenic Shock | 237 | IABP vs Impella CP and 2.5 | No difference in Mortality, Stroke |
↑Bleeding and ischemic complications inImpella group compared to IABP group | ||||
Casassus et al. | Refractory cardiogenic shock from acute myocardial infartion | 22 | Impella 2.5 | Transfusion due to bleeding: 18.2% |
limb ischemia: 10% | ||||
aortic insufficiency: 5.6% | ||||
Joseph et al. | Acute myocardial infarction and cardiogenic shock | 180 | Impella 2.5 | Hemolysis: 8.9% |
No aortic regurgitation | ||||
Bleeding requiring transfusion: 15.6% | ||||
Vascular complication: 11.7% | ||||
Lauten et al. | Acute Myocardial Infarction and Cardiogenic Shock | 120 | Impella 2.5 | Major Bleeding 28.6% |
Hemolysis: 7.5% | ||||
Ouweneel et al | Acute myocardial infarction and cardiogenic shock | 48 | IABP vs Impella CP | Hemolysis: 8% |
No incidence of device failure | ||||
Device-related bleeding: 13% | ||||
Major Vascular complication: 4% | ||||
No significant difference in mortality |
Table 1. Safety and Efficacy of PVAD implantation35,36,37,38,39,40. IABP: Intra-aortic balloon pump, pRBC: packed red blood cells, FFP: fresh-frozen plasma, LVEF: left ventricular ejection fraction.
Complication | Diagnosis | Management | Prevention |
Acute Limb Ischemia | · Clinical: Decreased or absent pulses on limb, limb pain, change in color to pale, blue. | · Internal or External percutaneous bypass, restoring antegrade flow | · Routine assessment of distal pulses |
· Imaging: Minimal or no pulse via Doppler ultrasound. | · Removal of Impella device, re-insertion at another arterial site with less vascular disease if needed for hemodynamic support | · If distal pulse is compromised, recommend creation of external or internal bypass to restore flow | |
· Laboratory: elevation in lactate | |||
Vascular Pseudoaneurysm | · Clinical: large, pulsatile mass, painful at access site, +thrill/bruit | ·<2-3cm, may resolve spontaneously | · Meticulous access techniques including use of Ultrasound, Fluoroscopy and micro-puncture access |
· Imaging: Doppler Ultrasound | · Ultrasound-guided thrombin injection | ||
· Surgical intervention (rapid increase in size, peripheral neuropathy, distal/cutaneous ischemia) | |||
Bleeding (external hematoma or internal retroperitoneal bleed) | · Clinical: hypotension despite improved cardiac output, visible hematoma, suction alarms | · If hematoma or oozing around access site, reposition angle of Impella | · Meticulous access technique with Ultrasound, Fluoroscopy and micro-puncture sheath to prevent ‘high stick’ (prevents retroperitoneal bleed) and minimize access attempts (prevents hematoma) |
· Laboratory: ↓hemoglobin | · Low-pressure balloon inflation at site of bleeding or covered stent deployment in extreme cases | ||
· Imaging: CT scan without contrast to diagnose retroperitoneal bleed | · Coil embolization for retroperitoneal bleed | ||
Hemolysis | · Clinical: change in color of urine to dark yellow, brown. | · Reposition device, generally away from mitral leaflet | · Good Impella position with inlet away from mitral apparatus |
· Laboratory: ↑ plasma-free hemoglobin, lactate dehydrogenase, bilirubin. ↓ hemoglobin, haptoglobin. | · Decrease power level | ||
· Removal of device if requiring significant blood transfusions (> 2 units) or causing renal function compromise. |
Table 2. Complications of PVAD15,41. Diagnosis and management of complications that arise from use of left-sided PVADs.
Minimizing the Risks and Complications of PVAD (Table 2)
The hemodynamic benefits of PVAD can be significantly neutralized if complications from large-bore access occur, such as major bleeding and acute limb ischemia28,29. It is thus essential to minimize the risk and complications of the device.
In order to decrease access site complications and reduce the number of access attempts, ultrasound and fluoroscopic guidance should be used when obtaining femoral arterial access10,30. Use of micropuncture allows operators to minimize trauma if the access is deemed to be at an inappropriate site9. Performing an aorto-iliac angiogram prior to placement of PVAD also helps in selecting the more favorable access site15. Vascular closure devices and endovascular balloon tamponade are effective in achieving hemostasis in patients with large-bore access and should be utilized whenever possible at the time of device removal15, 31.
Acute limb ischemia is a catastrophic complication of PVAD use. Assessing distal pulses in the extremity is a crucial step in early detection limb ischemia. If pulses are noted to be diminished from baseline or are absent, it is imperative to restore flow prior to the patient leaving the cardiac catheterization laboratory. The ability to create an external bypass circuit for limb perfusion is thus critical15. Based upon a patient's vascular anatomy an external ipsilateral, an external contralateral, or an internal contralateral circuit can be created15. Similarly, the ability to obtain and manage an alternative access point such as an axillary artery or transcaval access is essential in patients with PAD in an effort to avoid the risk of limb ischemia7,8.
Hemolysis can occur in patients treated with PVAD. In the EUROSHOCK registry hemolysis was present in 7.5% of patients28. Hemolysis can result in anemia, acute kidney injury and result in activating a systemic inflammatory response. Repositioning the PVAD device to clear the inlet from the mitral apparatus and decreasing the P level (at the cost of decreased flow) may help mitigate hemolysis.
Utilizing Shock Protocols
The aforementioned best practices led to the conceptualization and implementation of shock protocols for the treat of AMI-CS32. The use of these protocols has demonstrate improved survival when compared to historical controls (Figure 2)14. Quality measures such as PVAD utilization pre-PCI, door to support times, establishment of TIMI III flow in the culprit artery, utilization of right heart catheterization, the ability to wean vasopressors and inotropes and the ability to maintaining CPO > 0.6 Watts, are systemically evaluated and reported to improve outcomes within these institutions. However, while this data shows improved survival compared to prior studies, this data largely stems from single-arm registry rather than randomized controlled trials.
Limitations of the PVAD
There are several limitations to using PVADs. Severe PAD may limit implantation options, as access may occlude the vessel and lead to limb ischemia14. For example, if bilateral femoral disease or bypasses are present, the device may need to be placed either via the axillary artery or by transcaval access7,8,15. As with other ventricular assist devices, PVADs should not be used in patients with moderate to severe aortic regurgitation, as this device will worsen the aortic regurgitation rather than achieving the desired unloading of the LV12. Finally, for the left-sided PVADs, presence of an LV thrombus is an absolute contraindication due to the risk of stroke or other embolic events12. Furthermore, an Impella CP may not provide enough cardiac output, requiring upgrade to a larger PVAD or ECMO. Finally, a long-term plan should be considered for the patient – if the patient is not a candidate for advanced therapy (bridge to transplant or LVAD), then the likelihood of recovery and the duration of PVAD use should be discussed with the patient and/or family, heart failure specialist and interventionalist.
Limitations in the data
The aforementioned studies have been significantly limited in the number of patients, and in their retrospective, observational nature. Many are based on of registries, which allow for more confounding factors. There is as yet no large-scale prospective trial which demonstrates mortality benefit of the any MCS device in AMI-CS, though these studies are currently under way33.
Future Studies
Future studies evaluating the use of PVAD in AMI-CS must come from well powered randomized control trials. These efforts are already underway. The DanGer Shock Trial will be the first adequately powered randomized controlled trial in AMI-CS and will compare standard AMI-CS practice versus standard practice with PVAD33,34.
With increasing utilization of PVAD in AMI-CS it is important for clinicians to identify how to place, manage and wean such devices. In this article we have summarized how to place this device, step-by-step and best practices associated with improved outcomes when utilizing such devices. Formalizing these best practices based on local experience and expertise is encouraged until data from future well-powered trials is available.
The authors have nothing to disclose.
None
4 Fr-018-10 cm Silhouette Stiffened Micropuncture Set | Cook | G48002 | Microvascular access |
5 Fr Infiniti Pigtail Catheter | Cordis | 524-550S | pigtail catheter |
Impella CP Intra-cardiac Assist Catheter | ABIOMED | 0048-0003 | Impella catheter kit |